The lead content of most tissues is directly proportional to lead exposure. However, experimental studies suggest that kidney lead deposition accelerates as exposure increases while both epidemiological and experimental studies demonstrate that blood and urine lead concentrations show decreasing incremental rises with increasing exposure. Together with limited evidence for the development of lead tolerance, these observations suggest that internal redistribution and sequestration of lead responsive to lead exposure are mechanisms whose purpose is to reduce lead toxicity. The experiments described are designed to reproduce the nonlinearity of blood and kidney lead in an animal model and to use the model to: 1) study tissue distributions as functions of duration and magnitude of exposure, 2) study subcellular distributions in critical tissues as functions of duration and magnitude of exposure, 3) correlate these data with the results of tolerance studies to determine whether redistribution and sequestration are mechanisms of tolerance development, and 4) correlate the distribution data with response measures to determine whether the effect of lead is associated with an active fraction or fractions of the total body burden.